Publications by authors named "Yiyuan Kang"

An imbalanced system of angiogenesis-osteoblasts-osteoclasts is regarded as the main factor in bone remodeling dysfunction diseases or osseointegration loss. Osteoclast precursors are the key cells that accelerate bone-specific angiogenesis and maintain normal osteoblast and osteoclast function. Graphene oxide is an effective scaffold surface modification agent with broad application prospects in bone tissue engineering.

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Nanomaterials are widely utilized in several domains, such as everyday life, societal manufacturing, and biomedical applications, which expand the potential for nanomaterials to penetrate biological barriers and interact with cells. Multiple studies have concentrated on the particular or improper utilization of nanomaterials, resulting in cellular death. The primary mode of cell death caused by nanotoxicity is programmable cell death, which includes apoptosis, ferroptosis, necroptosis, and pyroptosis.

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Tissue engineering and regenerative medicine hold promise for improving or even restoring the function of damaged organs. Graphene-based materials (GBMs) have become a key player in biomaterials applied to tissue engineering and regenerative medicine. A series of cellular and molecular events, which affect the outcome of tissue regeneration, occur after GBMs are implanted into the body.

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During pregnancy, the human body is quite vulnerable to external stimuli. Zinc oxide nanoparticles (ZnO-NPs) are widely used in daily life, and they enter the human body via environmental or biomedical exposure, thus having potential risks. Although accumulating studies have demonstrated the toxic effects of ZnO-NPs, few studies have addressed the effect of prenatal ZnO-NP exposure on fetal brain tissue development.

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Article Synopsis
  • Nanoparticles (NPs), particularly zinc oxide (ZnO), can travel to the brain via the tongue-brain pathway, impacting neuronal function.
  • Research indicates that ZnO NPs decrease taste sensitivity and impair taste aversion learning, signifying abnormal taste perception.
  • The study identifies neuroinflammation as a key factor, highlighting the activated JAK-STAT signaling pathway's role in disrupting synaptic transmission, and suggests blocking this pathway could mitigate these effects.
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Biological barriers are essential physiological protective systems and obstacles to drug delivery. Nanoparticles (NPs) can access the paracellular route of biological barriers, either causing adverse health impacts on humans or producing therapeutic opportunities. This Review introduces the structural and functional influences of NPs on the key components that govern the paracellular route, mainly tight junctions, adherens junctions, and cytoskeletons.

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Article Synopsis
  • Overproduction of reactive oxygen and nitrogen species (RONS) in the brain contributes to neurological diseases like Alzheimer's and Parkinson's by causing cell stress.
  • Research is focusing on nanomaterials (NMs) that can neutralize RONS to reduce this stress and potentially slow disease progression.
  • The review discusses NMs' mechanisms for combating RONS, strategies to improve their effectiveness, and the challenges faced in their application for treating neurological disorders.
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Synaptic plasticity is an important basis of learning and memory and participates in brain network remodelling after different types of brain injury (such as that caused by neurodegenerative diseases, cerebral ischaemic injury, posttraumatic stress disorder (PTSD), and psychiatric disorders). Therefore, improving synaptic plasticity is particularly important for the treatment of nervous system-related diseases. With the rapid development of nanotechnology, increasing evidence has shown that nanoparticles (NPs) can cross the blood-brain barrier (BBB) in different ways, directly or indirectly act on nerve cells, regulate synaptic plasticity, and ultimately improve nerve function.

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The application of graphene-family nanomaterials (GFNs) in neuromedicine has recently gained increased attention, but the associated exposure risk for synaptic function and the underlying mechanism remains obscure. The results of this study utilizing nanosized graphene oxide (nGO) suggest that they exert depressive effects on neurotransmission, mainly due to energy deficiency at synaptic contacts. Mitophagy is activated but fails to renew mitochondria and maintain mitochondrial-mediated energy metabolism because of blockage of autophagosome transport through the microtubule system from the axonal terminal to the soma.

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Article Synopsis
  • The article discusses how inorganic-based nanomaterials (NMs) interact with biological membranes, which is crucial for developing new therapies and understanding nanotoxicity.
  • It focuses on the effects of these NMs on key membrane systems, highlighting the complex relationships between NMs and biomolecules like membrane proteins and lipids.
  • The review outlines the mechanisms of these interactions and stresses the need to understand them to enhance the design of nanomaterials for drug delivery and other medical applications.
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The widespread use of nanomaterials (NMs) has raised concerns that exposure to them may introduce potential risks to the human body and environment. The liver is the main target organ for NMs. Hepatotoxic effects caused by NMs have been observed in recent studies but have not been linked to liver disease, and the intrinsic mechanisms are poorly elucidated.

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The aim of this study is to evaluate the biological safety of tantalum (Ta) particles and to further explore the effects of Ta particles on human monocyte toxicity and inflammatory cytokine expression. Human monocyte leukemia (THP-1) cells were cultured with Ta and hydroxyapatite (HA) particles. Cell counting kit-8 method was used to evaluate the cytotoxicity of Ta and HA particles.

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  • The endothelium plays a crucial role in regulating vascular health and can impact various diseases, making it an important factor when considering therapeutic approaches.
  • Carbon nanomaterials (CBNs) show promise in biomedical applications due to their customizable properties and safety, but their interactions with the endothelium significantly influence their effectiveness.
  • This work examines how CBNs affect endothelial barriers, explores the factors shaping CBN-endothelium interactions, and emphasizes the need for balancing treatment efficiency with safety, particularly considering the diverse nature of vascular endothelium under different health conditions.
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  • Cartilage defects in temporomandibular disorders (TMD) cause chronic pain and have healing challenges, but synovium-derived mesenchymal stem cells (SMSCs) show potential for cartilage repair.
  • Inflammatory conditions, such as those activated by IL-1, disrupt the chondrogenic potential of SMSCs by increasing MMP13 and reducing important cartilage markers while affecting cellular processes.
  • The study suggests that using rapamycin to promote autophagy can enhance the chondrogenesis of SMSCs despite inflammation, highlighting the regulatory role of GSK3 and proposing a novel approach for treating TMD.
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Zinc oxide nanoparticles (ZnO-NPs) have been extensively applied in our daily life. Humans are at high risk of being exposed to ZnO-NPs, which induce potentially adverse health effects. Although a growing number of studies have investigated the toxic effects of ZnO-NPs, the available data concerning ZnO-NP interactions with the blood-milk barrier (BMB) remain highly limited.

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Neurotransmission is the basis of brain functions, and controllable neurotransmission tuning constitutes an attractive approach for interventions in a wide range of neurologic disorders and for synapse-based therapeutic treatments. Graphene-family nanomaterials (GFNs) offer promising advantages for biomedical applications, particularly in neurology. Our study suggests that reduced graphene oxide (rGO) serves as a neurotransmission modulator and reveals that the cellular oxidation of rGO plays a crucial role in this effect.

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The pharmacological potential of nanotechnology, especially in drug delivery and bioengineering, has developed rapidly in recent decades. Ion channels, which are easily targeted by external agents, such as nanomaterials (NMs) and synthetic drugs, due to their unique structures, have attracted increasing attention in the fields of nanotechnology and pharmacology for the treatment of ion channel-related diseases. NMs have significant effects on ion channels, and these effects are manifested in many ways, including changes in ion currents, kinetic characteristics and channel distribution.

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Autophagy is a biological process that has attracted considerable attention as a target for novel therapeutics. Recently, nanomaterials (NMs) have been reported to modulate autophagy, which makes them potential agents for the treatment of autophagy-related diseases. In this study, zinc oxide nanoparticles (ZNPs) are utilized to evaluate NM-induced autophagy and debate the mechanisms involved.

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Background: The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known.

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Silicon-based materials and their oxides are widely used in drug delivery, dietary supplements, implants and dental fillers. Silica nanoparticles (SiNPs) interact with immunocompetent cells and induce immunotoxicity. However, the toxic effects of SiNPs on the immune system have been inadequately reviewed.

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The ability to surgically repair peripheral nerve injuries is urgently needed. However, traditional tissue engineering techniques, such as autologous nerve transplantation, have some limitations. Therefore, tissue engineered autologous nerve grafts have become a suitable choice for nerve repair.

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Article Synopsis
  • The study investigates the cytotoxic effects of different sizes of zinc oxide nanoparticles (ZnO NPs) on the nervous system, particularly in SHSY5Y cells.
  • It highlights the role of reactive oxygen species and the release of zinc ions in causing damage, including apoptosis and changes to the cell's structure.
  • Results indicate that larger ZnO NPs have greater toxic effects, emphasizing the need for further research on their safety and impact on human health.
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